Issues

Combining predictive structural modeling and in vitro T-cell screens reveals the limitations of standard hybrid protein engineering and enables the design of highly functional MHC-independent T-cell receptors.

Targeting KRAS in pancreatic cancer induces a resistant, highly differentiated cell state that serves as a reservoir for disease relapse, and cytoablative strategies aimed at this state offer a novel approach to combat resistance.

Analysis of clinical samples from patients with pancreatic cancer and preclinical models treated with KRAS inhibitors identifies diverse mechanisms of resistance and yields new insights for developing combination therapy strategies.

The receptor tyrosine kinase ROR2 defines the cellular identity of pancreatic precancerous lesions and confers aggressiveness and therapeutic resistance in cancer.

The RAS(ON) multi-selective inhibitor RMC-7977, with or without covalent RAS(ON)^G12C targeting, induces sustained regressions in KRAS-mutant NSCLC models, but long-term antitumor activity is curtailed by a mucinous tolerogenic transcriptional state.

The phase 1 trial of mRNA-4157, an individualized neoantigen therapy, demonstrated strong T-cell responses and manageable safety, showing promise as a novel cancer immunotherapy in patients with resected NSCLC or melanoma.

A high-sensitivity, low-cost cell-free DNA fragmentome test is validated in the population eligible for lung cancer screening, with the potential to prevent thousands of deaths if used to close screening shortfalls.

A nationwide, comprehensive molecular profiling project in Japan demonstrates improved survival for patients with advanced solid tumors who received matched therapy based on molecular profiling, advancing precision oncology.

A single cell–resolution catalog of the pleural mesothelioma tumor microenvironment uncovers new therapeutic targets and treatment stratification strategies for patients with this deadly disease.

m⁶A epitranscriptome profiling analysis of lung adenocarcinoma and non-neoplastic lung identifies EML4 as a hyper-methylated metastatic driver and a promising therapeutic target to prevent lung adenocarcinoma metastasis.